Hyperlipaemia and hepatic steatosis are the most salient features of alcohol-induced alterations of fat metabolism. Carnitine is known to enhance fat metabolism by facilitating the transport of fatty acids not only to the site of beta-oxidation in mitochondria, but also from one body pool to another. Carnitine has also been shown to reduce the hperlipaemia and fatty liver caused by starvation and lysine deficiency. The possibility of a similar ameliorating effect of carnitine in alcohol-induced hyperlipaemia and hepatic steatosis forms a basic hypothesis to be tested. We propose to define the role of carnitine and its precursors (lysine & methionine) in fat metabolism of alcoholic model by studyig; 1) the levels of carnitine, acyl carnitine, total lipids, triglycerides and free fatty acids in plasma, liver and skeletal muscle with and without treatment with carnitine and 2) the rate of carnitine biosynthesis. These studies will utilize the laboratory rat as an experimental animal model and employ the latest carnitine-methodologies. A nutritionally adequate liquid diet will be fed with and without ethanol and basic criteria of alcoholism will be established in terms of morphological and biochemical changes, for example levels of serum enzymes and plasma and hepatic lipids. Using conventional metabolic techniques, the levels of carnitine and acyl carnitines will be measured in blood, urine, liver and skeletal mucle of alcoholic rats. Carnitine biosynthetic ability of alcoholic live will be assessed in liver slices and in subcellular organelles. Carnitine and/or lysine plus methionine will be administered to alcoholic rats and parameters of fatty acid metabolism will be measured as described.